[Status of the hypothalamo-hypophyseal neurosecretory system in mice with anaphylactic shock caused by administration of homogenates of lung tissue from influenza virus-infected and non-infected animals].

A significant increase in the lethal action of the homogenates obtained from animals infected with APR/8/34 influenza virus, as compared to the non-infected mice, was established using an experimental anaphylactoid shock model in CBA and (CBA x C57Bl)F1 mice by administering the lung tissue homogenates obtained from syngeneic donors. This increase was directly related to the inoculation dose (3.5 and 5.5 lg ED50) and infection development terms (days 2-3 or 5 after inoculation) but was not directly virus-mediated. It was found that in generally non-specific action of the lung tissue homogenates from non-infected and influenza-infected mice on the cellular structures of the viscera (liver, lungs) causing their damage and animal death, the infected lung homogenates show certain selectivity toward the hypothalamo-hypophyseal-neurosecretory system (HHNS) by blocking its reaction in anaphylactoid shock development, impairing the transport of neurohormones and their release into the neurohemal complex. The fact that the tissue products from the focus of influenza infection may affect the central mechanisms responsible for hemostatic control is thus demonstrated.